tbuckley/cabot-search huggingface dataset:
Platelet Factor 4 Modulates Fibroblast Growth Factor 2 (FGF-2) Activity and Inhibits FGF-2 Dimerization
Authors: Catherine Perollet, Zhong Chao Han, Catherine Savona, Jacques Philippe Caen, Andreas Bikfalvi
Journal: Blood (1998)

Platelet factor 4 (PF-4) inhibits angiogenesis in vitro and in vivo. The mechanism of inhibition is poorly understood. We have investigated the mechanism of inhibition by examining the interaction of PF-4 and the fibroblast growth factor-2 (FGF-2)/fibroblast growth factor receptor (FGFR) system. PF-4 inhibited the binding of FGF-2 to high-affinity and low-affinity binding sites in murine microvascular endothelial cells (LEII cells) and proliferation. Maximum inhibition of binding to endothelial FGF receptors was observed at PF-4 concentrations between 5 and 10 μg/mL (half maximum inhibition at 0.6 μg/mL), and proliferation was completely inhibited at 2 μg/mL. At this concentration, PF-4 reduced internalization of125I–FGF-2 by threefold and delayed degradation. To gain insight into the mechanism of inhibition, we have analyzed the interaction of PF-4 with FGF-2/FGFR by using mutant heparan sulfate–deficient Chinese hamster ovary (CHO) cells transfected with the FGFR-1 cDNA (CHOm–FGFR-1) and by examining the direct interaction with FGF-2. In the absence of heparin, PF-4 inhibited binding of 125I–FGF-2 to CHOm–FGFR-1 cells in a concentration-dependent manner, although not completely. In the presence of heparin, PF-4 abolished totally the stimulatory effect of heparin. Furthermore, PF-4 complexed to FGF-2 and inhibited endogenous or heparin-induced FGF-2 dimerization. These results indicate that PF-4 interacts with FGF-2 by complex formation, inhibiting FGF-2 dimerization, binding to FGF receptors, and internalization. This mechanism most likely contributes to the antiangiogenic properties of PF-4.
Incorrect Treatment Group in Results and Error in Legend of Figure 2
Authors: Andrew Armstrong, Orjan Nordle, Michael Morris
Journal: JAMA Oncology (2018)

Paolo A. Ascierto, MD; Georgina V. Long, MBBS; Caroline Robert, MD; Benjamin Brady, MD; Caroline Dutriaux, MD; Anna Maria Di Giacomo, MD; Laurent Mortier, MD; Jessica C. Hassel, MD; Piotr Rutkowski, MD; Catriona McNeil, MD; Ewa Kalinka-Warzocha, MD; Kerry J. Savage, MD; Micaela M. Hernberg, MD; Celeste Lebbé, MD; Julie Charles, MD; Catalin Mihalcioiu, MD; Vanna Chiarion-Sileni, MD; Cornelia Mauch, MD; Francesco Cognetti, MD; Lars Ny, MD; Ana Arance, MD; Inge Marie Svane, MD, PhD; Dirk Schadendorf, MD; Helen Gogas, MD; Abdel Saci, PhD; Joel Jiang, PhD; Jasmine Rizzo, MD, MPH; Victoria Atkinson, MD
Isoniazid Prophylaxis
Authors: WILLIAM W. STEAD
Journal: Annals of Internal Medicine (1981)

Letters and Corrections1 September 1981Isoniazid ProphylaxisWILLIAM W. STEAD, M.D.WILLIAM W. STEAD, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-95-3-393_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The analysis by Taylor and associates (1) of the benefit-risk ratio of recommending isoniazid to persons up to 35 years of age with a positive tuberculin reaction and no other risk factors is interesting and provocative. In the same issue Dr. Comstock has dealt at length with its major defects: minimizing the benefits while exaggerating the potential risk by drawing heavily on the unusual experience in Baltimore during the U.S. Public Health Service trial (2).The younger the age at which a positive tuberculin reaction is incidentally discovered, the greater is the chance the infection is recent...References1. TAYLORARONSONDELBANCO WMT. Should young adults with a positive tuberculin test take isoniazid? Ann Intern Med. 1981;94:808-13. LinkGoogle Scholar2. COMSTOCK G. Evaluating isoniazid preventive therapy: the need for more data. Ann Intern Med. 1981;94:817-9. Editorial. LinkGoogle Scholar3. STEADTEXTER WE. Isoniazid hepatitis: backlash of progress. Ann Intern Med. 1973;79:125-7. Editorial. LinkGoogle Scholar4. STEAD W. Undetected tuberculosis in prison: source of infection for community at large. JAMA. 1978;240:2544-7. CrossrefMedlineGoogle Scholar5. STEAD W. Tuberculosis among elderly persons: an outbreak in a nursing home. Ann Intern Med. 1981;94:606-10. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Arkansas Department of Health Little Rock, AR 72201 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTuberculosis Screening and Treatment of New York City Homeless People 1 September 1981Volume 95, Issue 3Page: 393-393KeywordsFactor analysisIsoniazidMedical risk factorsMedical servicesProphylaxisTuberculin ePublished: 1 December 2008 Issue Published: 1 September 1981 PDF downloadLoading ...
Long-term ganciclovir chemotherapy for congenital duck hepatitis B virus infectionin vivo: Effect on intrahepatic-viral DNA, RNA, and protein expression
Authors: C Luscombe, J Pedersen, E Uren, S Locarnini
Journal: Hepatology (1996)

Long–term antiviral chemotherapy using the nucleoside analogue ganciclovir was undertaken with the aim of eliminating hepadnaviral covalently closed circular (CCC) DNA from the livers of ducks that were congenitally infected with the duck hepatitis B virus (DHBV). Twenty– four weeks of ganciclovir therapy caused a substantial reduction in viremia, intrahepatic viral DNA replicative intermediates, and viral core proteins. Unfortunately, ganciclovir therapy did not substantially affect CCC DNA or viral RNA levels, and the treatment resulted in an increase in the intrahepatic expression of the viral envelope proteins, pre–S and S. By the completion of therapy, the viral envelope proteins had assembled into large aggregates within the cytoplasm of most hepatocytes. Viral replication in the bile duct epithelial cells and in the extrahepatic sites was likewise not affected by long–term ganciclovir therapy. In conclusion, 24 weeks of ganciclovir therapy decreased most viral replication markers within the liver, except for those of viral CCC DNA, RNA, and envelope proteins. Long–term therapeutic strategies using nucleoside analogs such as ganciclovir should be used with caution in chronic hepatitis B virus (HBV) infection. The careful monitoring of serum and hepatic markers of viral replication may therefore be important to avoid possible toxic consequences, such as the selective accumulation of viral proteins.
A SOFT RUBBER TIP FOR THE BELL TYPE OF STETHOSCOPE
Journal: JAMA (1921)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Topical Action of Salicylates in Gastrointestinal Erosion and Hemorrhage
Journal: JAMA (1963)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
ANGI-11. TUMOR TREATING FIELDS (TTFIELDS) INHIBIT CANCER CELL MIGRATION AND INVASION BY INDUCING REORGANIZATION OF THE ACTIN CYTOSKELETON AND FORMATION OF CELL ADHESIONS
Authors: Rosa S Schneiderman, Moshe Giladi, Einav Zeevi, Tali Voloshin, Anna Shteingauz, Yaara Porat, Mijal Munster, Eilon Kirson, Uri Weinberg, Yoram Palti
Journal: Neuro-Oncology (2018)

TTFields have been demonstrated to disrupt cancer cell replication in cultures, inhibit tumor progression in animals and increase overall survival in GBM patients when combined with temozolomide. TTFields are delivered via continuous, noninvasive application of low intensity, intermediate frequency alternating electric fields. In this study, we investigated the effects of TTFields on cancer cell migration and invasion properties. Glioma, breast, colon, melanoma and NSCLC cancer cell lines were treated with TTFields using the inovitro and the inovitro live systems. Cell migration rates were measured using wound healing assays. Invasion assays were performed using a modified Matrigel coated Boyden chamber. Cell adhesion assays were performed during TTFields treatment and compared to untreated controls. At the end of TTFields' treatment, adhered cells were trypsinized and counted. A cell de-adhesion assay was performed following different durations of TTFields application with the outcome being the number of cells removed after varying times of trypsinization. Confocal fluorescence microscopy imaging of vinculin and F-actin were utilized to demonstrate changes in cellular focal adhesions and stress fibers respectively following TTFields application. Application of TTFields in-vitro led to a significant reduction in the velocity of cell migration compared with untreated control cells. Cancer cell invasion was significantly reduced compared to untreated cells in all tested cell lines. In addition, cell de-adherence following TTFields treatment took significantly longer time of trypsinization. TTFields application also resulted in an increase in focal adhesion size and number as well as peripheral distribution of the adhesion sites. TTFields treated cells also adopted a more flattened and spread shape and exhibited reduction in appearance of stress fibers and a dense meshwork of actin filaments around the entire cell periphery. While typically regarded as an anti-mitotic treatment modality, TTFields may warrant further investigation and development for their anti-invasive and anti-metastatic potential.
Error in References
Authors: Katherine Rediger, D Miles, Seth Berkowitz, Jean Terranova, John Hsu, Cecil Sheps
Journal: JAMA Internal Medicine (2019)

In Reply We appreciate the thoughtful letter from Rediger and Miles regarding our study 1 and offer a few additional points.Given the importance of nutrition for health, we share the view that a broad range of nutrition options should be available to patients.In our view, medically tailored meal programs are one important tool that we hope becomes more widely available.Improving our knowledge regarding interventions to address food insecurity is an ongoing process, but we believe that implementation of existing interventions can cooccur with the further expansion of this evidence base.For example, Community Servings, in partnership with the Center for Health Law and Policy Innovation at Harvard Law School, is leading the development of a Food is Medicine State Plan in Massachusetts. 2 The goal of this plan is to not only address the nutritional needs of individuals through the health care system, but also to foster education, advocacy, and systems change regarding nutrition needs.An opportunity to help put this plan into action is coming in January 2020, when the Massachusetts Medicaid system will introduce financing mechanisms that allow for a broad array of beneficiary nutrition services, including medically tailored meals in appropriate circumstances.Nationwide, a major opportunity for similar work is that Medicare Advantage plans now have the ability to cover nutritional services via changes enacted in the Creating High-Quality Results and Outcomes Necessary to Improve Chronic Care Act. 3lthough meeting individual-level health-related social needs, such as food and nutrition, is a vital component of care, we also think it is important to view unmet health-related social needs as the end result of many social and environmental factors that affect health.Addressing these social determinants of health goes beyond clinical programs for individuals and requires collaboration among health care systems, public health systems, government, human services organizations, local communities, and families.Ultimately, we think it is critical not only to provide the appropriate services for those in need, but also to understand, and address, why health-related social needs arise.
Metabolism in Cancer
Journal: JAMA (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
miscellaneous and unclassified plans
Journal: JAMA (1959)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Two-dimensional real-time shear wave elastography and risk for de novo hepatocellular carcinoma in patients with advanced chronic liver disease
Authors: Wenyi Gu, Victor de Lédinghen, Christophe Aubé, Aleksander Krag, Christian Strassburg, Laurent Castéra, Jérôme Dumortier, Mireen Friedrich-Rust, Stanislas Pol, Ivica Grgurevic, Rong-Qin Zheng, Sven Francque, Halima Gottfriedova, Ioan Sporea, Cristina Margini, Christophe Cassinotto, Jerome Boursier, Ditlev Rasmussen, Valérie Vilgrain, Aymeric Guibal, Stefan Zeuzem, Camille Vassord, Luisa Vonghia, Renata Senkerikova, Alina Popescu, Annalisa Berzigotti, Wenping Wang, Maja Thiele, Christian Jansen, Jonel Trebicka
Journal: Journal of Hepatology (2020)
Abstract 17213: Does Left Ventricular - Mitral Ring Mismatch Predict Risk of Recurrent Mitral Regurgitation Post Annuloplasty in Patients With Ischemic Mitral Regurgitation?
Authors: ROMAIN CAPOULADE, Xin Zeng, Jessica R Overbey, Gorav Ailawadi, John Alexander, Deborah Ascheim, Michael Bowdish, Annetine Gelijns, Paul Grayburn, Irving Kron, Michael Mack, Serguei Melnichouk, Robert Michler, John Mullen, Patrick O'Gara, Michael Parides, Peter K Smith, Pierre Voisine, Judy Hung
Journal: Circulation (2015)

Background: In ischemic mitral regurgitation (IMR), ring annuloplasty is associated with a 30-50% rate of recurrent IMR. Ring size is based on inter-trigonal distance without consideration of LV size. However, LV size is an important determinant of mitral valve (MV) leaflet tethering pre and post repair. We aimed to determine if LV - MV ring mismatch (mismatch of LV size relative to ring size) is associated with recurrent IMR in patients post ring. Methods: Patients with moderate or severe IMR from the two cardiothoracic surgical network IMR trials (NCT-00806988 and 00807040) who received MV repair were examined at 1-year post-surgery. Baseline LV size was assessed by LV end-diastolic (LVIDed) and end-systolic (LVIDes) dimensions. LV- MV ring mismatch was calculated by dividing LV size by ring size (LVIDed/ring and LVIDes/ring). Multivariable regression models for each of these measures adjusting for age, sex, baseline LVEF and severe IMR were used to determine association with recurrent (≥moderate) IMR at one year. Results: 1-year post ring, 45 (21%) of 216 repair patients had ≥moderate IMR. In univariate analysis, larger LVIDes (p=0.02) and higher LVIDes/ring (p=0.006) were associated with recurrent IMR; LVIDed and LVIDed/ring was not (p&gt;0.05). In multivariable models both LVIDes/ring (p=0.01) and LVIDes (p=0.02) remained significantly associated with 1-year IMR recurrence; the odds of recurrence increasing by a relative 72% per 10% increase in LVIDes/ring and by 70% per 10mm increase in LVIDes. Conclusion: We found that increasing LV-MV ring mismatch and LVIDes are both associated with increased risk of IMR recurrence. The high correlation between LVIDes and LVIDes/ring in our data precludes a definitive determination of the relative contribution of each measure to the increased risk of IMR recurrence. While further research is needed to confirm our findings, these data may be helpful in guiding ring size to prevent recurrent IMR in patients undergoing MV repair.
Miscellany
Journal: JAMA (1934)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
The Papanicolaou Test and Screening for Cervical Cancer
Authors: Robert S. Scott
Journal: JAMA (1997)

<h3>To the Editor.</h3> —We agree with the assessment by Drs Austin and McLendon of the pressure that the Papanicolaou (Pap) test is receiving from both the medicolegal and cost-conscious managed care environments.<sup>1</sup>However, we are not certain that as clinicians we should simply continue to fight for the Pap test as the "proven" approach to screening for cervical neoplasia. In a meta-analysis of the literature on the Pap test, Fahey et al<sup>2</sup>have shown that when cervical biopsy is used as the reference for whether a cervical cancer or precancer is present, the overall sensitivity of the Pap test alone in detecting these lesions is between 20% and 35%, not 80% to 90% as presented by Austin and McLendon in their Editorial. We believe the screening accuracy reported in the Editorial may be overestimated and disagree that improving quality in the cytopathology laboratory will improve most of the
Antibody producing capacity to the bacteriophage phi X174 in yersinia arthritis.
Authors: R Bucknall, M Leirisalo-Repo, O Laitinen, J V Jones
Journal: Annals of the Rheumatic Diseases (1987)

Antibody production in response to the primary immunogen bacteriophage phi X174 was investigated in 14 patients with previous yersinia arthritis (YA) and in 15 controls. HLA-B27 occurred in 10 patients with YA and in three controls. After primary and secondary immunisation the antibody responses were essentially similar both in patients with YA and controls. Consequently our results suggest that antibody response to a foreign antigen does not differ between patients with YA and a normal control population. In addition, there was no difference in peak antibody responses between individuals with HLA-B27 and those without HLA-B27.
BOOK REVIEW
Authors: A. THIBAULT
Journal: JNCI Journal of the National Cancer Institute (1993)

BOOK REVIEW Get access Mélanome Cutané et des Muquenses Superficielles Michéle M. Delaunay , ed. Paris : Masson , 1992 . 172 pp., illus. In French. $47.71. ISBN 2-225-82716-8 ALAIN THIBAULT, M.D., F.R.C.P.(C) ALAIN THIBAULT, M.D., F.R.C.P.(C) Clinical Pharmacology Branch, National Cancer Institute, National Institutes of HealthBldg. 10 Rm. 5A01 9000 Rockville Pike Bethesda, MD 20892 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 18, 15 September 1993, Page 1523, https://doi.org/10.1093/jnci/85.18.1523 Published: 15 September 1993